This study investigated the neuroprotective effects of epigallocatechin-3-gallate (EGCG) on CA1 neuronal death following status epilepticus (SE) in rats. EGCG attenuated SE-induced CA1 neuronal death and mitochondrial hyperfusion by upregulating glutathione peroxidase-1 (GPx1), preserving ERK1/2-DRP1-mediated mitochondrial fission, and inhibiting NF-κB S536 phosphorylation. ERK1/2 inhibition blocked EGCG's neuroprotective and mitochondrial effects, suggesting ERK1/2 activation is crucial for EGCG's mechanism.
Publisher
Antioxidants
Published On
Apr 20, 2023
Authors
Andrey V Kozlov, Sabzali Javadov, Natascha Sommer, Ji-Eun Kim, Tae-Hyun Kim, Tae-Cheon Kang
Tags
epigallocatechin-3-gallate
neuroprotection
status epilepticus
neuronal death
mitochondrial fission
glutathione peroxidase-1
ERK1/2
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